Wolff-Parkinson-White syndrome

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Accessory pathways during ventricular preexcitation
ECG image of a patient with WPW syndrome: the arrow shows a typical 'delta wave.
ECG image of WPW syndrome in lead V2: PQ interval - 0.10 s ; delta wave ; normal second half of QRS complex ; QRS complex - 0.16 s

Ventricular preexcitation syndrome Under physiological conditions, the atrial myocardium is electrically connected to the ventricular myocardium only via the bundle of His, which penetrates through the fibrous skeleton into the interventricular septum. The impulse from the SA node spreads as follows: SA node → internodal atrial junctions → AV nodebundle of His → bundles of Tawar → Purkinje fibers → ventricular myocardium.

In the case of preexcitation syndromes, in addition to the bundle of His, there is an another connection between the atria and the ventricles. These so-called ``accessory pathways (accessory conduction bundles) do not connect to the AV node, therefore there is ``no slowing down of conduction from the atria to the ventricles, which results in ``premature activation ( excitation) of the myocardium of the ventricles (→ ventricular preexcitation syndrome).

Accessory bundles directly connect the atria to the ventricles. In most patients with ventricular preexcitation syndrome, they are located in the left heart.

The 3 most well-known ventricular preexcitation syndromes include:

  1. WPW syndrome (Wolf-Parkinson-White syndrome);
  2. LGL syndrome (Lown-Ganong-Levine syndrome);
  3. Mahaim type of preexcitation.


Wolff-Parkinson-White syndrome (WPW) is the most common ventricular preexcitation syndrome. This is a cardiac arrhythmia in which the impulse (wave of depolarization) spreads from the atria to the ventricles outside of the AV node. The accessory path here consists of the so-called Kent's bundle (= pathological connection between atria and ventricles).

Etiology[edit | edit source]

In a small group of patients, the cause of WPW syndrome is a mutation of the ``PRKAG2 gene. This gene encodes a protein that is part of an enzyme called AMP-activated protein kinase (AMPK) [1].

There is also a familial form of WPW syndrome (AD inheritance), but it is extremely rare [2].

Symptoms[edit | edit source]

WPW syndrome can manifest itself with the following symptoms:

  • dizziness, syncope;
  • palpitations (feelings of a pounding heart);
  • a feeling of "shortness of breath", the need to "breathe".

Diagnostics[edit | edit source]

The diagnosis is based on the ECG picture. In WPW syndrome, the following changes are observed on the ECG:

  • shortening of the PQ (PR) interval → PQ ≤ 0.12 s (there is no delay of the depolarization wave in the AV node);
  • delta wave (the beginning of the QRS complex is deformed by a delta wave, the myocardium of the ventricles is overexcited);
  • the second half of the QRS complex is normal (the wave of depolarization that reached the ventricles via the bundle of Kent meets the wave of depolarization that reached the ventricles normally via the bundle of His);
  • QRS complex widening above 0.10 s (QRS complex widening may occur due to delta wave).

In symptomatic patients (WPW + tachyarrhythmia) an electrophysiological examination is also necessary.

Complications ==

Principle of orthodromic AV reentry tachycardia: the impulse reaches the ventricles via a physiological route (via the AV node), from which, however, an accessory pathway in the septum between the left atrium and the left through the ventricle (bundle of James) it returns to the atria, creating a reentry circuit leading to tachycardia.

Abnormal junction of the ventricles with the atria (bundle of Kent) may be associated with other arrhythmias. The most common is paroxysmal supraventricular tachycardia', less often permanent supraventricular tachycardia, rarely ventricular tachycardia. Very rarely, WPW syndrome can result in ventricular fibrillation and sudden cardiac death.

The danger lies in the formation of the so-called reentry circuit and the so-called AV reentry tachycardia (AVRT, atrioventricular reentry tachycardia) [3].

  • In the case of orthodromic AVRT, the wave of depolarization propagates from the atria to the ventricles normally via the bundle of His and back from the ventricles to the atria via the bundle of Kent (95%).
  • In the case of antidromic AVRT, the wave of depolarization spreads from the atria to the ventricles via the bundle of Kent and from the ventricles to the atria via the bundle of His (5%).

→ In both cases, the atria are reactivated and a pathological circuit is formed, which results in tachycardia.

Treatment[edit | edit source]

Asymptomatic patients' - treatment is not necessary (catheter ablation is indicated in patients with risky occupations: pilots, drivers, ...) [4].

Symptomatic patients [5]

  1. Cancellation of an acute paroxysm of tachyarrhythmia: antiarrhythmics I. or III. classes.
  2. Pharmacological treatment: single administration of an antiarrhythmic drug at the beginning of a tachycardia paroxysm or long-term regular antiarrhythmic therapy.
  3. Catheter ablation (as part of an electrophysiological examination): radiofrequency disruption of Kent's bundle.

Links[edit | edit source]

Related Articles[edit | edit source]

External links[edit | edit source]

References[edit | edit source]

  1. U.S. National Library of Medicine. Medline plus [online]. [cit. 2010-11-14]. <https://ghr.nlm.nih.gov/condition/wolff-parkinson-white-syndrome>.
  2. U.S. National Library of Medicine. Medline plus [online]. [cit. 2010-11-14]. <https://ghr.nlm.nih.gov/condition/wolff-parkinson-white-syndrome>.
  3. FIALA, Martin. Recommended procedures for the diagnosis and treatment of supraventricular tachyarrhythmias. Cor et Vasa [online]2005, vol. 9, no. Supplement, p. 18-39, Available from <http://www.kardio-cz.cz/resources/upload/data/23_31-Guidelines-supraventrikularni_tachyarytmie.pdf/>. ISSN 1803-7712. 
  4. FIALA, Martin. Recommended procedures for the diagnosis and treatment of supraventricular tachyarrhythmias. Cor et Vasa [online]2005, vol. 9, no. Supplement, p. 18-39, Available from <http://www.kardio-cz.cz/resources/upload/data/23_31-Guidelines-supraventrikularni_tachyarytmie.pdf/>. ISSN 1803-7712. 
  5. FIALA, Martin. Recommended procedures for the diagnosis and treatment of supraventricular tachyarrhythmias. Cor et Vasa [online]2005, vol. 9, no. Supplement, p. 18-39, Available from <http://www.kardio-cz.cz/resources/upload/data/23_31-Guidelines-supraventrikularni_tachyarytmie.pdf/>. ISSN 1803-7712. 

References[edit | edit source]

  • TROJAN, Stanislav. Medical Physiology. 4th edition. Prague : Grada, 2004. 772 pp. ISBN 80-247-0512-5.
  • HELLO, Robert. Cardiology ring. III. internal clinic of VFN and 1st Faculty of Medicine of the University of Prague in Prague, 2009.
  • VILIKUS, Zdeněk. Interpretation of ECG at rest and during exercise. Institute of Physical Education Medicine 1. LF UK and VFN; 2010.